ArticleMediators of inflammation2013
Activation of protease-activated receptor 2-mediated signaling by mast cell tryptase modulates cytokine production in primary cultured astrocytes.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- Mast Cell-Microglia Crosstalk Drives Aberrant Synaptic Pruning Through PAR-2/MAPK/NF-κB Signaling in Neonatal Hypoxic-Ischemic Encephalopathy.CNS neuroscience & therapeutics · 2026Article
- Bidirectional Interplay Between Microglia and Mast Cells.International journal of molecular sciences · 2025Review
- Mast cell deficiency improves cognition and enhances disease-associated microglia in 5XFAD mice.Cell reports · 2023Article
- Involvement of kallikrein-PAR2-proinflammatory pathway in severe trastuzumab-induced cardiotoxicity.Cancer science · 2022Article
- Knockdown of PAR2 alleviates cancer-induced bone pain by inhibiting the activation of astrocytes and the ERK pathway.BMC musculoskeletal disorders · 2022Article
- Genetic Regulation of Tryptase Production and Clinical Impact: Hereditary Alpha Tryptasemia, Mastocytosis and Beyond.International journal of molecular sciences · 2021Review
- Inhibition of PAR-2 Attenuates Neuroinflammation and Improves Short-Term Neurocognitive Functions Via ERK1/2 Signaling Following Asphyxia-Induced Cardiac Arrest in Rats.Shock (Augusta, Ga.) · 2020Article
- Inhibition of mast cell tryptase attenuates neuroinflammation via PAR-2/p38/NFκB pathway following asphyxial cardiac arrest in rats.Journal of neuroinflammation · 2020Article
- Effect of tryptase on mouse brain microvascular endothelial cells via protease-activated receptor 2.Journal of neuroinflammation · 2018Article
- Histamine upregulates the expression of histamine receptors and increases the neuroprotective effect of astrocytes.Journal of neuroinflammation · 2018Article
- Emerging Roles of Immune Cells in Postoperative Cognitive Dysfunction.Mediators of inflammation · 2018Review
- Thalamic mast cell activity is associated with sign-tracking behavior in rats.Brain, behavior, and immunity · 2017Article
- Therapeutic innovation: Inflammatory-reactive astrocytes as targets of inflammation.IBRO reports · 2016Article
- Regulation of Calcium-Independent Phospholipase A2 Expression by Adrenoceptors and Sterol Regulatory Element Binding Protein-Potential Crosstalk Between Sterol and Glycerophospholipid Mediators.Molecular neurobiology · 2016Article
- In vitro model of the blood-brain barrier established by co-culture of primary cerebral microvascular endothelial and astrocyte cells.Neural regeneration research · 2015Article
- Evaluation on potential contributions of protease activated receptors related mediators in allergic inflammation.Mediators of inflammation · 2014Review
- Targeting mast cells tryptase in tumor microenvironment: a potential antiangiogenetic strategy.BioMed research international · 2014Review
- Abnormal interactions between perifollicular mast cells and CD8+ T-cells may contribute to the pathogenesis of alopecia areata.PloS one · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protease-activated receptor 2 (PAR-2), which is abundantly expressed in astrocytes, is known to play major roles in brain inflammation. However, the influence of the natural agonist of PAR-2, tryptase, on proinflammatory mediator releasedfrom astrocytes remains uninvestigated. In the present study, we found that tryptase at lower concentrations modestly reduced intracellular ROS production but significantly increased IL-6 and TNF- α secretion at higher concentrations without affecting astrocytic viability and proliferation. The actions of tryptase were alleviated by specific PAR-2 antagonist FSLLRY-NH2 (FS), indicating that the actions of tryptase were via PAR-2. PI3K/AKT inhibitor LY294002 reversed the effect of tryptase on IL-6 production, whereas inhibitors specific for p38, JNK, and ERK1/2 abolished the effect of tryptase on TNF- α production, suggesting that different signaling pathways are involved. Moreover, tryptase-induced activation of MAPKs and AKT was eliminated by FS, implicating that PAR-2 is responsible for transmitting tryptase biosignals to MAPKs and AKT. Tryptase provoked also expression of TGF- β and CNTF in astrocytes. The present findings suggest for the first time that tryptase can regulate the release of cytokines from astrocytes via PAR-2-MAPKs or PAR-2-PI3K/AKT signaling pathways, which reveals PAR-2 as a new target actively participating in the regulation of astrocytic functions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.